This review highlights the role of insulin resistance and postprandial triglyceride-rich lipoproteins in driving endothelial dysfunction and cardiovascular risk in Type 2 diabetes.
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Should not alter T2D management; leaves open whether targeting postprandial lipoproteins improves endothelial outcomes.
Recent evidence from prospective epidemiological large-scale studies have providedconvincing proof for the role of nonfasting triglycerides, carried in VLDL and chylomicrons,as an independent risk factor for cardiovascular disease and death. Overproduction oflarge VLDL1 by the liver on one hand, and accumulation of apoB-48-containing triglyceriderichlipoproteins (TRLs) on the other hand are present before overt hyperglycemia,highlighting the role of insulin resistance as an early pathogenic defect. Multiple insulinaction sites demonstrate insulin resistance in the liver, adipose tissue and muscle, as well asin the intestine. Together, these perturbations of insulin action contribute to theoverproduction of atherogenic VLDL and chylomicron remnant particles. Consequently, thevascular wall endothelium is exposed to exaggerated cholesterol influx resulting inendothelial dysfunction, oxidative stress and prothrombotic state during subsequent mealsover the 24-h period. This overview summarizes current understanding of diabeticpostprandial ‘dysmetabolism’ and reviews recent data on TRL secretion and intravascularprocessing and removal accumulated during this decade. Various therapeutic strategiesand future opportunities are also discussed.
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Matikainen et al. (2008) studied this question.
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